Hypertensive Disorders And Cardiac Disease In Pregnancy

Question 1

Hypertensive disorders during
pregnancy are classified into

Answer 1

Hypertensive disrders in preg are divided into 4 categories:
a) Gestational hypertension
b) Chronic hypertension
c) Chronic hypertension with superimposed preeclampsia
d) Preeclampsia-eclampsia

Question 2

Hypertension in pregnancy

Answer 2

 Hypertension in pregnancy is
defined as either:
 A blood pressure of more than
140/90 mmHg on 2 occasions
more than 4-6 hours apart.
 A diastolic >110 mmHg on
one occasion
 A rise of more than 30 mmHg
in systolic blood pressure over
the booking pressure.
 A rise of more than 15mmHg
in diastolic blood pressure
over the booking figure.

Question 3

Criteria for dsis of superimposed
pre-eclampsia

Answer 3

(i) New onset of proteinuria >0.5
gm/24 hours specimen.
(ii) Aggravation of hypertension.
(iii) Thrombocytopenia or
(iv) Raise of liver enzymes

Question 4

Common causes of chronic hypertension:

Answer 4

(a) Essential hypertension
(b) Chronic renal disease (reno vascular)
(c) Coarctation of aorta
(d) Endocrine disorders (diabetes mellitus, pheochromocytoma,
thyrotoxicosis
(e) Connective tissue diseases (Lupus erythematosus)

Question 5

Preeclampsia

Answer 5

 A multisystem progressive disorder of unknown etiology characterized by new onset of HTN to the extent of
140/90 mmHg or more with proteinuria after 20th wk GA in a previously normotensive & nonproteinuric woman.
 New-onset HTN & end-organ dysfunction with / without proteinuria, in last 1
/2 of preg /postpartum, preeclampsia
can be diagnosed if there is evidence of 1 or more of the following abnormalities: thrombocytopenia or DIC,
elevated transaminases or other signs of hepatic injury, CNS symptoms, an elevated or rising serum
creatinine level, or pulmonary edema.
 Edema is not part of diagnostic criteria unless it is pathological as eadema is common in normal preg
 In hydatidiform mole and acute Polyhydramnios, preeclamptic features may appear even before 20th week

Question 6

Clinical types of Preeclamsia

Answer 6

 Types principally are based on blood pressure level and significant proteinuria
1) Mild preeclampsia: sustained rise of BP of > 140/90 mmHg but <160 mm Hg systolic or 110 mm Hg
diastolic without significant proteinuria.
 PE without severe features
 Diagnosed when severe disease is ruled out
2) Severe preeclapsia:
 Persistent SBP of ≥160 or DBP of ≥110 mmHg.
 Heavy proteinuria- of ≥ 0.3gm/24 hr urine
 Oliguria (<400 ml/24 hr).
 Platelet count < 100,000/mm3
 HELLP syndrome  Thrombocytopenia
 Cerebral or visual disturbances
 Persistent sev epigastric pain/ rt upper quadrant pain
 Retinal hemorrhages, exudates or papilledema
 Intrauterine growth restriction of the fetus
 Pulmonary edema hypoxia/cyanosis
 Hepatic dysfunction (elevated liver enzymes)

Question 6

Risk factors for pre-eclampsia

Answer 6

a) Primigravida: Young or elderly (first time exposure to chorionic villi)
b) Advanced maternal age (maternal age > 35 years)
c) Family history: Hypertension, pre-eclampsia
d) Chronic Hypertension
e) Chronic renal disease
f) Placental abnormalities:
 Hyperplacentosis (placenta is enlarged): Excessive exposure to chorionic villi-(molar preg, DM, hydrops)
g) Placental ischemia: results in oxidative and inflammatory stress, with involvement of secondary mediators
leading to endothelial dysfunction, vasospasm, and activation of the coagulation system.
 Hypoxic placenta may also shed microparticles derived from apoptosis of syncytiotrophoblasts, which then
lead to widespread endothelial injury.
h) Diabetes (pregestational and gestational)
i) Obesity: BMI >35 kg/M2, Insulin resistance.
j) Multiple pregnancy
k) Multiparous with:
 Pre-eclampsia in any previous pregnancy
 Prolonged interpregnancy interval- ten years or more interval, if previous preg was normotensive
l) Pre-existing vascular disease- Pre-existing hypertension, renal diseases
m) Thrombophilias (, protein C, S deficiency, Factor V Leiden)
n) Autoimmune disorders (antiphospholipid syndrome, SLE)
o) New paternity (new partner)
p) In vitro fertilisation
q) Black race
NB: Smoking dencreases the risk of preeclampsia

Question 7

Etiopathological factors for pre-eclampsia

Answer 7

a) Failure of trophoblast invasion (abnormal placentation)
b) Vascular endothelial damage
c) Inflammatory mediators (cytokines)
d) Immunological intolerance betwn maternal & fetal tissues
e) Coagulation abnormalities
f) Increased oxygen free radicals
g) Genetic predisposition (polygenic disorder)
h) Dietary dieficiency or excess

Question 8

Pathophysiology for preeclampsia

Question 9

Systemic Effect of PE

Answer 9

1) CVS- Marked peripheral vasoconstriction, resulting in htn
 Endothelial dysfunction, increased permeability and contributes to formation of generalized oedema.
 Intense vasospasm impairs circulation in vasa vasorum leading to vascular walls damage
2) Renal system- glomeruloendotheliosis (characteristic atherosclerotic-like changes in renal vessels)  impairs
glomerular filtration lead to proteinuria, reduced uric excretion & oligouria (increasing serum creatinine)
3) Haematological system- Endothelial damage cause platelet aggregationthrombocytopenia, DIC, HELLP
syndrome
 Third spacing of fluid (evidenced by pitting edema) is due to→
a) Hypoproteinuria  ↓oncotic pressure transudation of intravascular fluid into interstitium  oedema
 haemoconcentration risk of hypovolemic shock if hemorrhage occurs
b) Increased blood pressure
c) Endothelial dysfunction increase permeability
4) Neurological system- Vasospasm and cerebral oedema headache, visual symptons (blurred vision, scotomas),
Hyperreflexia/hypersensitivity and convulsions (eclampsia)
 Retinal haemorrhages, exudates and papilloedema are characteristic of hypertensive encephalopathy
5) Pulmonary effects: Decreased oncotic
pressure and pulmonary capillary leak and
Left heart failure → pulmonary edema
6) Liver - thrombosis of arterioles → periportal
hemorrhagic necrosis of liver starts at
periphery of the lobule
 Subcapsular hemorrhage.
 Subendothelial fibrin deposition is associated with elevation of liver enzymes, haemolysis and a low platelet
count due to platelet consumption

Question 10

HELLP Syndrome

Answer 10

 Acronym for Hemolysis (H), Elevated Liver enzymes (EL) and Low Platelet count (LP) (<100,000/mm3).
 Rare complication of PE (10–15%). HELLP syndrome may develop even without maternal htn.
 Prompt recognition is vital to improving outcomes
 Manifest with nausea, vomiting, epigastric or rt upper quadrant pain, along with biochemical, & hematological changes
 Parenchymal necrosis of the liver causes elevation in hepatic enzymes (AST and ALT >70 IU/L, LDH >600
IU/L) and bilirubin (>1.2 mg/dL).
 There may be subcapsular hematoma formation (diagnosed by CT scanning) and abnormal peripheral bld smear.
 Eventually liver may rupture to cause sudden hypotension, due to hemoperitoneum

Question 10

 Complications of HELLP syndrome

Answer 10

 Maternal:
a) Abruptio placenta
b) DIC
c) Acute renal failure,
d) Severe ascites,
e) Pulmonary edema,
f) Pleural effusions,
g) Cerebral edema,
h) Laryngeal edema,
i) Retinal detachment,
j) Subcapsular liver hematoma,
k) ARDS,
l) Sepsis, and
m) Maternal mortality.
 Perinatal:
a) Preterm delivery-prematurity,
b) RDS
c) Sepsis

Question 11

 Management of HELLP Syndrome

Answer 11

 Antiseizure prophylaxis with magnesium sulphate
 Fetal and maternal assessment before delivery
 Give corticosteroid to improve perinatal (↑ pulmonary maturity, ↓ IVH and ↓NEC) and maternal (↑
thrombocyte count, ↑ urinary output) outcome
 Platelet transfusion should be given if the count is <50,000/mm3

Question 12

Complications of pre-eclampsia

Answer 12

Maternal
During pregnancy:
 Eclampsia (2%)
 Accidental hemorrhage, Abruptio placenta
 Oliguria and anuria,
 Dimness of vision and even blindness,
 Preterm labor,
 HELLP syndrome
 Cerebral hemorrhage,
 ARDS due to “leaky” pul capillaries leading to pulmonary edema
During labor:
a) Eclampsia,
b) Postpartum hemorrhage - coagulation failure
Puerperium:
a) Eclampsia - usually occurs within 48 hours,
b) Shock - puerperal vasomotor collapse is associated with reduced concentration of sodium and chloride due to
sudden fall in corticosteroid level
c) Sepsis - due to increased incidence of induction, operative interference, and low vitality
Remote
1. Residual hypertension:may persist even after 6 months following delivery in about 50% cases
2. Recurrent pre-eclampsia: in subsequent pregnancies
3. Chronic renal disease

FETAL EFFECTS: vasospasm decreases placental perfusion causing
(A) IUGR- due to chronic placental insufficiency
(B) IUFD- due to spasm of uteroplacental circulation leading to accidental hemorrhage or acute infarction,
(C) Oligohydramnios
(D) Increase perinatal mortality
(E) Increased incidence of nonreassuring fetal status in labor (results from inability of placenta to oxygenate fetus during contractions)
(a) Prematurity- either due to spontaneous preterm onset of labor or due to preter induction.

Question 13

Clinical features of preeclampsia

Answer 13

 PE is principally a syndrome of signs and when symptoms appear, it is usually late
 Majority are asymptomatic
 Mild symptoms:
a) Frontal headache,
b) Visual disturbance and
c) Epigastric pain or pain in rt upper quadrant
 Ominous symptoms- occuring singly or in combination.
a) Headache- either occipital or frontal region
b) Disturbed sleep,
c) Diminished urinary output -Urinary output of < 400 ml in 24 hours
d) vomiting
e) Epigastric & rt abdominal pain- due to hemorrhagic gastritis or due to subcapsular hemorrhage in liver
f) Eye symptom - may be:
 Blurring vision
 Scotomata
 Dimness of vision or at times complete blindness
Signs
a) Abnormal weight gain
b) Rise of BP
c) Edema:
d) ARDS due to Pulmonary edema
e) Abdominal examination may reveal scanty liquor or IUGR with HOF < GA due to chronic
placental insufficiency
f) Hyperreflexia and clonus (> 3 beats) in severe cases.
g) Proteinuria
h) Decreased Fundal height
NB: Course of PE appear in following order- usually insidious in onset and runs a slow course→ rapid weight
gain → visible edema and/or hypertension → proteinuria→late detection/untreated→Eclampsia
 PE detected early: with effective treatment, pre-eclamptic features may subside completely

Question 14

untreated preeclampsia

Answer 14

a) Preeclamptic features may remain stationary at varying degrees till delivery
b) Aggravation of features
c) Eclampsia- following acute fulminating PE or bypassing it
d) Rarely, spontaneous remission of preeclamptic features

Question 15

Investigations for Pre-eclampsia

Answer 15

1. Urine examination: for proteinuria, pus cells, RBCs, casts, specific gravity, M/C/S.
2. FBC- Anaemia, thrombocytopenia
    ↓hematocrit may signify hemolysis, & ↑HCT reflects relative hypovolemia and hemoconcentration
3. Kidney function tests:
    Serum uric acid ((biochemical marker of PE) > 6 mg % is abnormal during preg
    Serum creatinine level and Blood urea level remains normal or slightly raised.
4. LFT and Biochem – increased liver enzymes (ALT, AST of >70 U/L), ↑bilirubin (1.2mg/dl), ↓Albumin
5. Hemolysis-Abnormal PBS, ↑Indirect bilirubin level over 1.2 mg/dL, ↑LDH level > 600 U/L
6. Coagulation status: Platelet count, FDP, Elevated PT or aPTT, decreased fibrinogen due to DIC.
7. Ophthalmoscopic examination:
8. Antenatal fetal monitoring done by
    Clinical examination,
    Daily fetal kick count
    U/Sound for fetal growth, fetal size & liquor vol
    Cardiotocography - non-stress test
    Umbilical artery flow velocimetry and
    Biophysical profile
    Oxytocin challenge test (if needed)
9. CT Scanning and MRI – Reveal cerebral edema, focal infarction, intracranial hemorrhage, and posterior
   leukoencephalopathy but not pathognomonic

Question 16

Severe features of preeclampsia include…?

Answer 16

b) Proteinuria- ≥ 300mg per 24hrs urine collection, protein/creatinine ≥0.3mg/dL or urinalysis of ≥ 1+ proteinuria (if
quantitative measurements are unavailable
c) Thrombocytopenia (platelet count less than 100,000/microliter)
d) Impaired liver function- with elevated liver enzymes (transaminase) atleast twice their normal conc
e) Progressive renal insufficiency with Oliguria <500 mL in 24 hours/ creatinine conc ≥1.1mg/dL
f) New onset cerebral or visual disturbances
g) Pulmonary edema
h) Epigastric or right upper quadrant pain”

Question 17

Pre-eclampsia prophylactic measures in potentially high risk women

Answer 17

a) Regular antenatal check up for early detection of rapid gain in weight or a tendency of rising BP.
b) Antithrombotic agents: Low dose aspirin 75 mg OD beginning early in pregnancy.
MOA: Aspirin selectively reduces platelet thromboxane production by inhibiting cyclo-oxygenase in platelets
thereby preventing the formation of thromboxane A2 without interfering with prostacyclin generation.
c) Heparin or LMW heparin is useful in those with thrombophilia and with high risk pregnancy.
d) Calcium supplementation (2 gm per day) reduces the risk of gestational hypertension.
e) Antioxidants - vits E and C and nutritional supplementation with mg, zinc, fish oil and low salt diet have been
tried but are of limited benefit.
f) Balanced diet rich in protein may reduce the risk.

Question 18

Objectives of Management of pre-eclampsia

Answer 18

 Delivery of fetus and placenta is the only definitive cure for preeclampsia
 Treatment depends on
a) Severity of the disease process
b) Evidence of fetal compromise (i.e., IUGR, oligohydramnios, or heart rate abnormalities)
c) GA and fetal maturity.
 Objectives are:
a) To stabilise HTN and to prevent its progression to SPE.
b) To prevent complications
c) To prevent eclampsia.
d) Delivery of a healthy baby at optimal time.
e) Mother’s health restoration in puerperium
 For mild PE, without evidence of fetal compromise, and not severe or not progressing, will generally not be
delivered unless GA is ≥ 37 weeks
 But for SPE or eclampsia at ≤ 34 weeks’ gestation should be delivered regardless of the GA.
 There is no place of domiciliary treatment in an established case of preeclampsia

Question 19

Management of pre-eclampsia

Answer 19

 Expectant management is permitted in uncomplicated mild pre-eclampsias and pregnancy is < 34 weeks
 Warn pt on ominous symptoms; headache, visual disturbances, vomiting, epigastric pain or scanty urine
 Bed rest: often in left-lateral position to lessen effects of vena caval compression.
* Rest increases renal blood flow, uterine blood flow, improves placental perfusion, and reduces BP.
 Diet: with adequate protein, no salt & fluid restriction
 Diuretics: used judiciously as it endangers fetus by diminishing placental perfusion & electrolyte imbalance
* Only indicated in: Pulmonary edema, cardiac failure, & massive edema- refractory to rest & causing discomfort
* Commonly used is frusemide (Lasix) 40mg p.o for 5 days in a week. Preferably IV in acute conditions
 Corticosteroid- Give Dexamethasone 6mg im twice 12hrs apart, to enhance lung maturity.
 Antihypertensives: to control BP due to preeclampsia.
a) Methyldopa p.o is a centrally acting antihypertensive agent.
b) Labetalol p.o/iv is an α-blocking and β blocking agent.
c) Nifedipine is a Ca-channel blocker with a rapid onset of action
 If pre-eclamptic features subside and hypertension is mild- but duration of preg is remote from termdischarge and review in antenatal clinic after 1 week
 If < 37 wks, expectant treatment may be extended judiciously at least up to 34 weeks.
 Monitoring
* Daily clinical evaluation for any symptoms (e.g. headache, epigastric pain, visual disturbances, oliguria).
* BP: at least four times a day.
* State of edema and daily wgt record.
* Fluid intake and urinary output.
* Daily urinalysis- for protein and estimate its amount in 24 hours urine.
* Bld for HCT, platelet count, uric acid, creatinine and LFT at least once a wk.
* Ophthalmoscopic examination on admission and to be repeated, PRN.
* Fetal well-being assessment-
 Daily kick fetal chart,
 FHR daily,
 Twice weekly CTG-Non stress or biophysical profile
 Serial ultrasound for growth every 2 -4 weeks, liquor vol etc.

Question 20

Management for severe preeclampsia-

Answer 20

 Counsel couple for TOP (delivery) irrespective of duration of gestation.
 Definitive treatment of SPE is termination of pregnancy (delivery).
 Start seizure prophylaxis (magnesium sulfate) to prevent eclampsia
 Consider steroid therapy if duration of preg is < 34 weeks to prevents neonatal RDS, IVH, NEC and maternal
thrombocytopenia.
 Antihypertensives – as above but doses can be titrated.
 Fetal assessment
i. Daily NST
ii. Continue serial U/S for growth and fluid assessment

Question 21

Indications for delivery in preeclampsia

Answer 21

a) Worsening fetal status: Abnormal NST, development of IUGR and Oligohydramnios
b) Worsening of maternal status
i. Uncontrolled hypertension
ii. Evidence of end-organ compromise: P/Embolism, HELLP syndrome, ↓renal function, CNS symptoms,
coagulopathy
iii. Development of HELLP syndrome
iv. Eclampsia
c) Placenta abruption
d) Attainment of a gestational age of 34 weeks

Question 22

 Indications for induction of labor in SPE

Answer 22

a) Worsening of preeclamptic features and/or appearance of newer symptoms such as epigastric pain.
b) Uncontrolled Hypertension despite of medical treatment
c) Acute fulminating pre-eclampsia irrespective of the period of gestation
Method of ILO
 ILO: If cervix is ripe, surgical induction by low ROM is method of choice.
 Oxytocin infusion may be added
 If the cervix is unripe, PGE2 (dinoprostone) gel 500 µg intracervical or 1–2 mg posterior fornix is
inserted OR misoprotol 25mcg P.O, vaginally in the posterior fornix or rectally

Question 23

Cesarean section: Indications in preeclampsia

Answer 23

a) When urgent termination is indicated & cervix is unfavorable b) SPE associated with complicating factors, e.g. elderly PG, contracted pelvis, malpresentation. NB: Avoid ergometrine in 3 rd stage

Question 24

Acute fulminant pre-eclampsia (syn: preeclamptic state)

Answer 24

 It is a clinical entity where onset of preeclamptic manifestations is acute, occurring de novo or there is rapid deterioration in an established case of PE with severe htn over a short period of time.  Threat is onset of; convulsion, cerebral hemorrhage, cardiac failure or placental abruption.  All the features of severe pre-eclampsia are intensified

Question 25

Tx of preeclamptic state

Answer 25

Treatment:  Adequately sedate pt with pethidine 75–100 mg or diazepam 10 mg im, refer to specialist and handle pt gently  Institute Prophylactic anticonvulsant therapy urgently- Mg sulphate iv/im  Antihypertensive drugs to control BP  Monitor treatment responce by noting frequently BP, urinary output, proteinuria and hematological parameters. Obstetric management:  Due to constant threat of eclampsia, consider maternal interest always.  Preg beyond 37th completed wks or condition not improving within a period (6–8 hours), delivery irrespective of period of gestation.  Termination is either by low ROM aided by oxytocin infusion or by c/section depending on severity of condition and state of cervix. PGE2 gel may help in cervical ripening.  Give corticosteroid if pregnancy is < 34 weeks.

Question 26

Eclampsia

Answer 26

 Eclampsia- is PE complicated with generalized tonic–clonic convulsions &/or coma  May occur quite abruptly, without any omnious features of SPE, but in 80% of cases is preceded by SPE  Is a life threatening complications of SPE, defined as tonic, clonic convulsions in a pregnant woman in the absence of any other neurological or metabolic causes.  May occur in pts with Preeclampsia or in pts who have PE superimposed on chronic htn or chronic nephritis.  Common in PG (75%), 5X more common in twin than singleton preg & occurs betwn 36th wk & term in > 50%  Frequency of occurance is; antepartum (before onset of labour- (50%), intrapartum (30%), during labor and postpartum- puerperium (after delivery 24-48hs) - (20%)  Fits occurring beyond 48hrs but <4 wks after delivery is accepted as late postpartum eclampsia

Question 27

Eclampsia Cause of convulsion

Answer 27

 Cause of cerebral irritation leading to convulsion is not clear.  Vasospasm and cerebral oedema are both implicated in the pathogenesis of eclampsia.  The irritation may be provoked by: a) Anoxia - spasm of the cerebral vessels → increased cerebral vascular resistance → fall in cerebral oxygen consumption→ anoxia b) Cerebral edema - may contribute to irritation c) Cerebral dysrhythmia- increases following anoxia or edema leading to excessive release of excitatory neurotransmitters (glutamate)  Cerebral pathology includes cortical or subcortical edema, infarction and hemorrhage. Neurological abnormalities are often due to hypoxia, ischemia or edema

Question 28

Clinical features of eclampsia

Answer 28

 An eclamptic pt usually show previous acute fulminating pre-eclampsia manifestations- called premonitory symptoms  Eclamptic convulsions or fits are epileptiform and consist of 4 stage a) Premonitory stage: Pt becomes unconscious, twitching of muscles of face, tongue, and limbs, eyeballs roll or are turned to one side and become fixed. Stage lasts for about 30 seconds. b) Tonic stage: Whole body goes into a tonic spasm-trunk-opisthotonus, limbs are flexed and hands clenched, resp ceases and tongue protrudes betwn teeth. Cyanosis appears. Eyeballs are fixed. Lasts for about 30 sec c) Clonic stage: All voluntary muscles undergo alternate contraction and relaxation. Twitchings start in face then involve one side of extremities and ultimately the whole body. lasts for 1–4 minutes d) Stage of coma: Following the fit, pt passes on to the stage of coma  When fit occurs in quick succession, it is called status eclampticus

Question 29

Differential diagnosis of Eclampsia

Answer 29

 Exclude diseases associated with convulsions and/or coma, such as; a) Epilepsy, b) Hysteria, c) Cerebral thrombosis, d) Poisoning, e) Cerebral malaria in tropics, f) Intracranial tumors. g) Encephalitis, h) Meningitis, NB: Puerperal absence of previous H/O convulsion with presence of edema, htn& proteinuria along with fits or coma during pregnancy or soon after, points to diagnosis of eclampsia

Question 30

Principles of management of eclampsia

Answer 30

a) Maintain: airway(suction, oro-pharyngeal sirway), breathing & circulation b) Oxygen administration 8–10 L/min c) Hemodynamic stabilization (control BP - hydralazine, labetalol) d) IV access – With two large bore canulas e) Organize investigations (urinalysis, RFT- (urea, creatinine), FBC, LFT, clotting profile, cross match. f) Arrest convulsions - (magnesium sulphate, diazepam) g) Deliver by 6-8 hours - after pt stabilization, control of BP, convulsions and hypoxia h) Ventilatory support (if needed) i) Prevention of complications j) Prevention of injury k) Postpartum care (intensive)

Question 31

Management of Eclampsia

Answer 31

 Obstetric managt: depends on- (i) whether fits are controlled or not (ii) maturity of fetus. But do delivery fast  Often eclampsia is preceded by SPE and so its prevention rests on early detection and effective treatment with judicious termination of pregnancy during pre-eclampsia.  At times, eclampsia occurs bypassing the preeclamptic state and as such, it is not always a preventable condition  Use of antihypertensive drugs- Labetalol 20 mg IV to control hypertension, hydralazine, nifedipine  Prophylactic anticonvulsant therapy- MgSO2  Abort seuzures, diazepam or phenobarbitone  Timely delivery  Fits controlled and baby is mature- delivery  Fits not controlled with anticonvulsant within (6–8 hours), TOP should be done  Status eclampticus: Thiopentone Na 0.5 gm dissolved in 20 mL of 5% dextrose is given iv  Pulmonary edema: Furosemide 40 mg IV followed by 20 g. of mannitol IV reduces pulmonary edema and also prevents ARDS  Heart failure: Oxygen inhalation, parenteral Lasix and digitalis  Anuria: Dopamine infusion (1 µg/kg) is given with oliguria when CVP is >8 mmHg  Hyperpyrexia: Temperature is difficult to bring down as it is central in origin. However, cold sponging and antipyretics may be tried.  Psychosis: Chlorpromazine or Eskazine (trifluoperazine) is quite effective.  Intensive care monitoring: Turn the patient on her side  Monitor- Intake & output chart- Fluid balance:  Crystalloid solution (R/L) is a first choice.  Total fluids not to exceed previous 24hrs urinary output plus 1000 ml  Catheterise pt and do urinalysis for protein.  Monitor maternal and fetal well-being- Half hrly pulse, respiration rates & BP are recorded, FHR  Antibiotic: To prevent infection, Ceftriaxone 1 gm IV twice daily is give

Question 32

Magnesium sulphate

Answer 32

 Drug of choice in eclampsia  Dose is 4-6g loading dose, 1-2g maintenance IV/IM  Over dose lead to respiratory depression and cardiac arrest  Repeat doses are only given if: knee jerks are present, urine output exceeds 30 mL/hr and RR is >12 per minute  And should be continued for 24 hours after the last seizure or delivery  S/Effects: respiratory depression, depressed reflexes, hypotesion, diaphoresis, oliguria etc  Monitor patient (reflexes, RR, urine output)  Antidote calcium gluconate 10ml 10%.  No detrimental effects on neonate within therapeutic level  Its not an anti-hypertensive

Question 33

Magnesium sulphate MOA

Answer 33

a) Acts as a membrane stabilizer and (cerebral vasodilator) neuroprotector. b) Reduces motor end-plate sensitivity to acetylcholine. c) Blocks neuronal calcium influx also. d) Induces cerebral vasodilatation, dilates uterine arteries, increases production of endothelial prostacyclin and inhibits platelet activation

Question 34

Maternal complications of eclampsia

Answer 34

1) Injuries:  Tongue bite, injuries due to fall from bed, bed sore. 2) Pulmonary complications:  Edema- due to leaky blood capillaries  Pneumonia - due to aspiration, hypostatic or infective  ARDS  Embolism Hyperpyrexia  Cardiac - Acute left ventricular failure  Renal failure  Hepatic- necrosis, Subcapsular hematoma  Cerebral: Edema (vasogenic) hemorrhage  Neurological deficits  Disturbed vision: Due to retinal detachment or occipital lobe ischemia.  Hematological  Thrombocytopenia  DIC  Postpartum  Shock  Sepsis  Psychosis

Question 35

Prognosis of eclampsia

Answer 35

Maternal:  Once the convulsion occurs, the prognosis becomes uncertain.  Prognosis depends on many factors and the ominous features are: a) Long interval between the onset of fit and commencement of treatment b) Antepartum eclampsia esp with long delivery interval c) Number of fits > 10 d) Coma in between fits e) Temperature over 102°F with pulse rate above 120/minute f) Blood pressure over 200 mm Hg systolic g) Oliguria (< 400 mL/24 hours) with proteinuria > 5 gm/24 hours. h) Nonresponse to treatment i) Jaundice.

Question 36

Maternal causes of deaths in eclampsia

Answer 36

a) Cardiac failure. g) Cardiopulmonary arrest. b) Pulmonary edema. h) Adult respiratory distress syndrome (ARDS). c) Aspiration and/or septic i) Pulmonary embolism d) Pneumonia j) Postpartum shock. e) Cerebral hemorrhage. k) Puerperal sepsis f) Acute renal failure. Maternal complications are higher in antepartum eclampsia

Question 37

Fetal causes of deaths in eclampsia

Answer 37

Fetal causes of deaths: perinatal mortality is about 30–50%. a) Prematurity- spontaneous or induced b) Intrauterine asphyxia due to placental insufficiency arising out of infarction, retroplacental hemorrhage and spasm of uteroplacental vasculature, c) Effects of the drugs used to control convulsions, d) Trauma during operative delivery

Question 38

Gestational hypertension

Answer 38

 A sustained rise of BP ≥ 140/90 mm Hg on at least 2 occasions, 4 or more hours apart beyond 20th week of GA or during the 1st 24 hrs after delivery in a previously normotensive woman  Diagnosis is made if; HTN without proteinuria or no other signs of organ dysfunction 1st appears after 20 weeks’ gestation or within 48 to 72 hours of delivery and resolves by 12 weeks postpartum.

Question 39

Criteria for diagnosis of gestational Hypertension

Answer 39

 Absence of underlying cause of hypertension  Unassociciated with features of pre-eclampsia (edema or proteinuria).  Majority of cases are > 37 weeks pregnancy  Not associated with hemoconcentration, thrombocytopenia, raised serum uric acid level or hepatic dysfunctn.  BP should normalise within 6 weeks following delivery

Question 40

Chronic hypertension in pregnancy (CHD)

Answer 40

 Defined as the presence of hypertension of any cause antedating or before the 20th week of pregnancy and its presence beyond the 12 weeks after delivery.  Overall incidence: is 2–4% of which 90% are due to essential hypertension

Question 41

Chronic hypertension in pregnancy high risk factors

Answer 41

 High risk factors for CHD are: a) Age (> 40 years) b) Duration of hypertension (>15 years) c) Level of BP (>160/110 mm of Hg) d) Presence of any medical disorder (renovascular) e) Presence of thrombophilias.

Question 42

ANTIHYPERTENSIVES AND PREGNANCY

Answer 42

 Methyl-dopa has been shown to be safe in pregnancy.  Labetalol and atenolol are acceptable alternative.  Beta-blocking agents are associated with intrauterine growth retardation (IUGR).  NEVER USE angiotensin-converting enzyme inhibitors as they are contraindicated in pregnancy they have been associated with fetal hypocalvaria, renal failure, oligohydramnios and death.  Diuretics should not be initiated during pregnancy owing to possible adverse fetal effects of associated plasma volume reduction.  BP target range: maintain diastolic values between 90 and 100mmHg.